ArticleFEBS open bio2020
CNOT7 depletion reverses natural killer cell resistance by modulating the tumor immune microenvironment of hepatocellular carcinoma.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- CCR4-NOT Transcription Complex Subunit 7 (CNOT7) Protein and Leukocyte-Associated Immunoglobulin-like Receptor-1 in Breast Cancer Progression: Clinical Mechanistic Insights and In Silico Therapeutic Potential.International journal of molecular sciences · 2025Article
- Oncogenic Gene CNOT7 Promotes Progression and Induces Poor Prognosis of Glioma.Molecular biotechnology · 2025Article
- Review
- Article
- The Roles of Epigenetic Regulation and the Tumor Microenvironment in the Mechanism of Resistance to Systemic Therapy in Hepatocellular Carcinoma.International journal of molecular sciences · 2023Review
- Circular RNA hsa_circ_001350 contributes to osteosarcoma progression by regulating microRNA-578/CCR4-NOT transcription complex and subunit 7/Wnt signaling.American journal of cancer research · 2023Article
- Overcoming the therapeutic resistance of hepatomas by targeting the tumor microenvironment.Frontiers in oncology · 2022Review
- Identify and Validate the Transcriptomic, Functional Network, and Predictive Validity of FBXL19-AS1 in Hepatocellular Carcinoma.Frontiers in oncology · 2020Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major obstacle to effective cancer immunotherapy is the tumor immune microenvironment. Natural killer (NK) cell resistance has been suggested as a primary cause of poor prognosis in hepatocellular carcinoma (HCC), which seemingly correlates with CNOT7 overexpression. CNOT7, a cytoplasmic mRNA deadenylase that is highly expressed in HCC, may regulate cytokine transforming growth factor-β1 (TGF-β1) secretion by controlling nuclear factor-κB subunit p65 trafficking. CNOT7 depletion suppresses TGF-β1 secretion in HCC and promotes interferon-γ (IFN-γ) secretion by NK cells, and we previously demonstrated that CNOT7 depletion reversed IFN-γ resistance in HCC cells. Therefore, we hypothesized that CNOT7 depletion might reverse NK cell resistance by influencing the tumor immune microenvironment of HCC. To test this hypothesis, we examined the correlation between CNOT7, STAT1, TGF-β1 and IFN-γ expression with hepatitis B virus-related cirrhosis and HCC with hepatitis B virus-related cirrhosis. We found that modulation of CNOT7 expression alters TGF-β1 secretion in HCC and IFN-γ secretion in NK cells. We also examined the effects of NK cells in HepG2 cells with CNOT7 knockdown, which showed that NK cell surface CD107a expression is up-regulated and caspase-3 expression is significantly enhanced in CNOT7-deficient HepG2 cells. Overall, our results show that knockdown of CNOT7 expression reverses NK cell resistance in HCC cells. Therefore, CNOT7 depletion has potential as a new adjuvant therapy in immunotherapy for HCC.
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